Genetic Variants and Atherosclerosis

Atherosclerosis is the condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.




References:
[1] Maton, Anthea, Roshan L,et al. Human Biology and Health. Englewood
Cliffs, New Jersey, USA: Prentice Hall. (1993); ISBN 0-13-981176-1.
OCLC 32308337
[2] Ridker PM. Inflammation, atherosclerosis, and cardiovascular risk: an
epidemiologic view. Blood Coagul Fibrinolysis. 1999;10(suppl 1):S9-
S12.
[3] Crouse JR, Grobbee DE, O-Leary DH, et al. Measuring effects on intima
media thickness: an evaluation of rosuvastatin in subclinical
atherosclerosisÔÇöthe rationale and methodology of the METEOR study.
Cardiovasc Drugs Ther. 2004;18:231-238.
[4] Viles-Gonzalez JF, Fuster V, Badimon JJ. Atherothrombosis: a
widespread disease with unpredictable and life-threatening
consequences. Eur Heart J. 2004;25: 1197-1207.
[5] Jensen LO,Thayssen P, Pedersen KE, et al. Regression of coronary
atherosclerosis by simvastatin: a serial intravascular ultrasound study.
Circulation. 2004;110: 265-270.
[6] Rauch U, Osende JI, Fuster V, et al. Thrombus formation on
atherosclerotic plaques: pathogenesis and clinical consequences. Ann
Intern Med. 2001;134:224-238.
[7] Ohashi R, Mu H,Yao Q, et al. Atherosclerosis: immunopathogenesis and
immunotherapy. Med Sci Monit. 2004; 10:RA255-RA260.
[8] Hansson GK. Inflammation, atherosclerosis, and coronary artery disease.
N Engl J Med. 2005;352: 1685-1695.
[9] Ben-Haim S, Israel O. PET/CT for atherosclerotic plaque imaging. QJ
Nucl Med Mol Imaging. 2006;50: 53-60.
[10] Van Mieghem CAG, McFadden EP, de Feyter PJ, et al. Noninvasive
detection of subclinical coronary atherosclerosis coupled with
assessment of changes in plaque characteristics using novel invasive
imaging modalities. The Integrated Biomarker and Imaging Study. J Am
Coll Cardiol. 2006;47:1134-1142.
[11] Weissberg PL. Atherogenesis: current understanding of the causes of
atheroma. Heart. 2000;83:247-252.
[12] Carlos TM , Harlan JM. Leukocyte-endothelial adhesion molecules.
Blood 1994;84:2068-101.
[13] Vora DK, Fang ZT, Liva SM, et al. Induction of P-selectin by oxidized
lipoproteins. Separate effects on synthesis and surface expression. Circ
Res 1997;80:810-8.
[14] Iiyama K, Hajra L, Iiyama M, et al. Patterns of vascular cell adhesion
molecule-1 and intercellular adhesion molecule-1 expression in rabbit
and mouse atherosclerotic lesions and at sites predisposed to lesion
formation. Circ Res 1999;85:199-207.
[15] Gu L, Okada Y, Clinton SK, et al. Absence of monocyte chemoattractant
protein-1 reduces atherosclerosis in low density lipoprotein receptordeficient
mice. Mol Cell 1998;2:275-81.
[16] Watson AD, Leitinger N, Navab M, et al. Structural identification by
mass spectrometry of oxidized phospholipids in minimally oxidized low
density lipoprotein that induce monocyte/endothelial interactions and
evidence for their presence in vivo. J Biol Chem 1997;272:13597-607.
[17] von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and
arteriosclerosis. Role of cholesterol efflux and reverse cholesterol
transport. Arterioscler Thromb Vasc Biol 2001; 21:13-27.
[18] Libby P, Warner SJ, Salomon RN, et al. Production of platelet-derived
growth factor-like mitogen by smooth-muscle cells from human
atheroma. N Engl J Med 1988;318:1493-8.
[19] Higashiyama S, Abraham JA, Miller J, et al. A heparin-binding growth
factor secreted by macrophage-like cells that is related to EGF. Science
1991;251:936-9.
[20] Libby P. Changing concepts of atherogenesis. J Intern Med 2000;
247:349-58
[21] Amento EP, Ehsani N, Palmer H, et al. Cytokines and growth factors
positively and negatively regulate interstitial collagen gene expression in
human vascular smooth muscle cells. Arterioscler Thromb
1991;11:1223-30
[22] van der Wal AC, Becker AE, van der Loos CM, et al. Site of intimal
rupture or erosion of thrombosed coronary atherosclerotic plaques is
characterized by an inflammatory process irrespective of the dominant
plaque morphology. Circulation 1994;89:36-44.
[23] Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix
metalloproteinases and matrix degrading activity in vulnerable regions
of human atherosclerotic plaques. J Clin Invest 1994;94:2493-503.
[24] Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s.
Nature 1993;362:801- 9.
[25] Libby P. Molecular bases of the acute coronary syndromes. Circulation
1995;91:2844- 50.
[26] Davies MJ. Stability and instability: two faces of coronary
atherosclerosis. The Paul Dudley White Lecture 1995. Circulation 1996;
94:2013-20.
[27] Hangartner JR, Charleston AJ, Davies MJ, Thomas AC. Morphological
characteristics of clinically significant coronary artery stenosis in stable
angina. Br Heart J 1986;56:501-8.
[28] Blankenhorn DH, Hodis HN (August 1993). "Atherosclerosis--reversal
with therapy". The Western journal of medicine 159 (2): 172-9. PMID
8212682.
[29] Botto N, Rizza A, Colombo M, Mazzone A, Manfredi S, Masetti S, et al.
Evidence for DNA damage in patients with coronary artery disease.
Mutat Res 2001;493:23- 30.
[30] Andreassi MG, Botto N, Cocci F, et al. Methylenetetrahydrofolate
reductase gene C677T polymorphism, homocysteine, vitamin B12, and
DNA damage in coronary artery disease. Hum Genet 2003;112:171-7.
[31] Botto N, Berti S, Manfredi S, et al. Detection of mtDNA with 4977bp
deletion in blood cells and atherosclerotic lesions of patients with
coronary artery disease. Mutat Res 2005;570:81- 8.
[32] Henney AM, Wakeley PR, Davies MJ, et al. Localization of stromelysin
gene expression in atherosclerotic plaques by in situ hybridization. Proc
Natl Acad Sci USA 1991;88:8154_/8.
[33] Galis, Z.S., Khatri, J.J., 2002. Matrix metalloproteinases in vascular
remodeling and atherogenesis: the good, the bad, and the ugly. Circ. Res.
90 (3), 251-262.
[34] Newby, A.C., 2005. Dual role of matrix metalloproteinases (matrixins)
in intimal thickening and atherosclerotic plaque rupture. Physiol Rev. 85
(1), 1-31.
[35] Newby, A.C., Johnson, J.L., 2005. Genetic strategies to elucidate the
roles of matrix metalloproteinases in atherosclerotic plaque growth and
stability. Circ. Res. 97 (10), 958-960.
[36] Hayashidani, S., Tsutsui, H., Ikeuchi, M., et al. Targeted deletion of
MMP 2 attenuates early LV rupture and late remodeling after
experimental myocardial infarction.2003; Am. J. Physiol. Heart Circ.
Physiol. 285 (3), H1229-H1235
[37] Heymans, S., Luttun, A., Nuyens, D., et al. Inhibition of plasminogen
activators or matrix metalloproteinases prevents cardiac rupture but
impairs therapeutic angiogenesis and causes cardiac failure. 1999;
Nature Med. 5 (10), 1135-1142.
[38] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S.,
Okada, Y., Targeted deletion or pharmacological inhibition of MMP-2
prevents cardiac rupture after myocardial infarction in mice. 2005a; J.
Clin. Invest. 115 (3), 599-609.
[39] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S.,
Okada, Y.,. Targeted deletion or pharmacological inhibition of MMP-2
prevents cardiac rupture after myocardial infarction in mice. 2005b; J.
Clin. Invest. 115 (3), 599-609.
[40] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection
from ischemia/reperfusion injury by targeted deletion of matrix
metalloproteinase-9. 2002a; Cardiovasc. Res. 54 (3), 549-558.
[41] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection
from ischemia/reperfusion injury by targeted deletion of matrix
metalloproteinase-9.2002b; Cardiovasc. Res. 54 (3), 549-558.
[42] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection
from ischemia/reperfusion injury by targeted deletion of matrix
metalloproteinase-9.2002c; Cardiovasc. Res. 54 (3), 549-558.
[43] Deschamps, A.M., Yarbrough, W.M., Squires, C.E., et al. Trafficking of
the membrane type-1 matrix metalloproteinase in ischemia and
reperfusion: relation to interstitial membrane type-1 matrix
metalloproteinase activity. 2005; Circulation 111 (9), 1166-1174.
[44] Fedak, P.W., Smookler, D.S., Kassiri, Z., et al. TIMP-3 deficiency leads
to dilated cardiomyopathy.2004; Circulation 110 (16), 2401-2409.
[45] Longo, G.M., Xiong, W., Greiner, T.C., Zhao, Y., Fiotti, N., Baxter,
B.T.,. Matrix metalloproteinases 2 and 9 work in concert to produce
aortic aneurysms. 2002; J. Clin. Invest. 110 (5), 625-632.
[46] Johnson, J.L., George, S.J., Newby, A.C., Jackson, C.L.,. Divergent
effects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic
plaque stability in mouse brachiocephalic arteries. 2005; Proc. Natl.
Acad. Sci. USA 102 (43), 15575-15580.
[47] Chase, A.J., Newby, A.C.,. Regulation of matrix metalloproteinase
(matrixin) genes in blood vessels: a multi-step recruitment model for
pathological remodelling. 2003; J. Vasc. Res. 40 (4), 329-343.
[48] Ye S, Watts GF, Mandalia S, Humphries SE, Henney AM. Preliminary
report: genetic variation in the human stromelysin promoter is associated
with progression of coronary atherosclerosis. Br Heart J 1995;73:209-
15.
[49] Ye S, Eriksson P, Hamsten A, Kurkinen M, Humphries SE, Henney AM.
Progression of coronary atherosclerosis is associated with a common
genetic variant of the human stromelysin-1 promoter which results in
reduced gene expression. J Biol Chem 1996;271:13055-60.
[50] Humphries S, Bauters C, Meirhaeghe A, Luong L, Bertrand M, Amouyel
P. The 5A6A polymorphism in the promoter of the stromelysin-1
(MMP3) gene as a risk factor for restenosis. Eur Heart J 2002;23:721-5.
[51] Seifi M, Fallah S, Firoozrai M. Influence of Genetic Polymorphism in
Matrix Metalloproteinase-3 on Extent of Coronary Atherosclerosis and
Risk of Coronary Artery Stenosis. Archives Medical Research. In press
[52] Primo-Parmo SL, Sorenson RC, Teiber J, La Du BN. The human serum
paraoxonase/arylesterase gene (PON1) is one member of a multigene
family. Genomics. 1996;33:498 -507.
[53] Watson AD, Berliner JA, Hama SY, La Du BN, Faull KF, Fogelman
AM, Navab M. Protective effect of high density lipoprotein associated
paraoxonase. Inhibition of the biological activity of minimally oxidized
low density lipoprotein. J Clin Invest. 1995;96:2882-2891.
[54] Ng CJ, Wadleigh DJ, Gangopadhyay A, Hama S, Grijalva VR, Navab
M, Fogelman AM, Reddy ST. Paraoxonase-2 is a ubiquitously expressed
protein with antioxidant properties and is capable of preventing
cellmediated oxidative modification of low density lipoprotein. J Biol
Chem. 2001;276:44444-44449.
[55] Li B, Sedlacek M, Manoharan I, Boopathy R, Duysen EG, Masson P,
Lockridge O: Butyrylcholinesterase, paraoxonase, and albumin esterase,
but not carboxylesterase, are present in human Plasma. Biochem
Pharmacol. 2005;70: 1673-1684.
[56] Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La
Du BN. Paraoxonase inhibits high-density lipoprotein oxidation and
preserves its functions: a possible peroxidative role for praoxonase. J
Clin Invest. 1998;101:1581-1590.
[57] Durrington P.N, Mackness B and Mackness M.I. Parooxonase and
atherosclerosis. Arterioscler.Tromb.Vasc.Biol.2001;21:473-480
[58] Kuremoto K, Watanabe Y, Ohmura H et al: R/R genotype of human
paraoxonase (PON1) is more protective against lipoprotein oxidation
and coronary artery disease in Japanese subjects. J Atheroscler Thromb,
2003; 10: 85-92
[59] Huang Y, Mironova M, Lopes-Virella MF: Oxidized LDL stimulates
matrix metalloproteinase-1 expression in human vascular endothelial
cells. Arterioscler Thromb Vasc Biol, 1999; 19: 2640-47
[60] Navab M, Berliner JA, Watson AD et al: The yin and yang of oxidation
in the development of fatty streak: a review based on the 1994 George
Lyman Duff Memorial Lecture. Arterioscler Thromb Vasc Biol, 1996;
16: 831-42
[61] Navab M, Hama SY, Anantharamaiah GM et al: Normal high-density
lipoprotein inhibits three steps in the formation of mildly oxidized low
density lipoprotein: steps 2 and 3. J Lipid Res, 2000; 41: 1495-508
[62] Mackness MI, Durrington PN: HDL, its enzymes and its potential to infl
uence lipid peroxidation. Atherosclerosis, 1995; 115: 243-53
[63] Watson AD, Berliner JA, Hama SY et al: Protective effect of high
density lipoprotein associated paraoxonase: inhibition of biological
activity of minimally oxidized low density lipoprotein. J Clin Invest,
1995; 96: 2882-91
[64] Blatter MC, James RW, Messmer S et al: Identifi cation of a distinct
human high-density lipoprotein subspecies defi ned by a lipoproteinassociated
protein, K-45: identity of K-45 with paraoxonase. Eur J
Biochem, 1993; 211: 871-79
[65] Kelso GJ, Stuart WD, Richter RJ et al: Apolipoprotein J is associated
with paraoxonase in human plasma. Biochemistry, 1994; 33: 832-39
[66] Humbert R, Adler DA, Disteche CM et al: The molecular basis of the
human serum paraoxonase activity polymorphism. Nat Genet, 1993; 3:
73-76
[67] Adkins S, Gan KN, Mody M, La du DN: Molecular basis for the
polymorphic form of human serum paraoxoanase/arylesterase: glutamine
or arginine at position 191, for the respective A or B allozymes. Am J
Hum Genet, 1993; 52: 598-60
[68] Fortunato G, Rubba P, Panico S, Trono D, Tinto N, Mazzaccara C, De
Michele M, Iannuzzi A, Vitale DF, Salvatore F, Sacchetti L. A
paraoxonase gene polymorphism, PON 1 (55), as an independent risk
factor for increased carotid intima-media thickness in middle-aged
women. Atherosclerosis. 2003;167:141-148.
[69] Markus H, Kapozsta Z, Ditrich R, Wolfe C, Ali N, Powell J, Mendell M,
Cullinane M. Increased common carotid intima-media thickness in UK
African Caribbeans and its relation to chronic inflammation and vascular
candidate gene polymorphisms. Stroke. 2001;32:2465-2471.
[70] Jarvik GP, Hatsukami TS, Carlson C, Richter RJ, Jampsa R, Brophy VH,
Margolin S, Rieder M, Nickerson D, Schellenberg GD, Heagerty PJ,
Furlong CE. Paraoxonase activity, but not haplotype utilizing the linkage
disequilibrium structure, predicts vascular disease. Arterioscler Thromb
Vasc Biol. 2003;1923:1465-1471
[71] Pallaud C, Sass C, Zannad F, Siest G, Visvikis S. APOC3, CETP,
fibrinogen, and MTHFR are genetic determinants of carotid intimamedia
thickness in healthy men (the Stanislas cohort). Clin Genet.
2001;59:316-324.
[72] Schmidt H, Schmidt R, Niederkorn K, Gradert A, Schumacher M,
Watzinger N, Hartung HP, Kostner GM. Paraoxonase PON1
polymorphism leu-Met54 is associated with carotid atherosclerosis:
results of the Austrian Stroke Prevention Study. Stroke. 1998;29:2043-
2048.
[73] Koch M, Hering S, Barth C, Ehren M, Enderle MD, Pfohl M.
Paraoxonase1 192 Gln/Arg gene polymorphism and cerebrovascular
disease: interaction with type 2 diabetes. Exp Clin Endocrinol Diabetes.
2001;109:141-145.
[74] Cao H, Girard-Globa A, Serusclat A, Bernard S, Bondon P, Picard S,
Berthezene F, Moulin P. Lack of association between carotid intimamedia thickness and paraoxonase gene polymorphism in noninsulin
dependent diabetes mellitus. Atherosclerosis. 1998;138: 361-366.
[75] Dessi M, Gnasso A, Motti C, Pujia A, Irace C, Casciani S, Staffa F,
Federici G, Cortese C. Influence of the human paraoxonase
polymorphism (PON1 192) on the carotid-wall thickening in a healthy
population. Coron Artery Dis. 1999;10:595-599.
[76] Jarvik GP, Rozek LS, Brophy VH, Hatsukami TS, Richter RJ,
Schellenberg GD, Furlong CE. Paraoxonase (PON1) phenotype is a
better predictor of vascular disease than is PON1(192) or PON1(55)
genotype. Arterioscler Thromb Vasc Biol. 2000;20:2441-2447.
[77] Leus FR, Wittekoek ME, Prins J, Kastelein JJ, Voorbij HA. Paraoxonase
gene polymorphisms are associated with carotid arterial wall thickness in
subjects with familial hypercholesterolemia. Atherosclerosis. 2000;
149:371-377.
[78] Sakai T, Matsuura B, Onji M. Serum paraoxonase activity and genotype
distribution in Japanese patients with diabetes mellitus. Intern Med.
1998;37:581-584.
[79] Gnasso A, Motti C, Irace C, Di G, I, Pujia A, Leto E, Ciamei M, Crivaro
A, Bernardini S, Federici G, Cortese C. The Arg allele in position 192 of
PON1 is associated with carotid atherosclerosis in subjects with elevated
HDLs. Atherosclerosis. 2002;164:289-295.
[80] Zuliani G, Cherubini A, Volpato S, Palmieri E, Mecocci P, De Rango P,
Cao P, Costantini F, Mezzetti A, Mascoli F, Senin U, Fellin R. Genetic
factors associated with the absence of atherosclerosis in octogenarians. J
Gerontol A Biol Sci Med Sci. 2002;57:M611-M615.
[81] Mackness MI, Arrol S, Mackness B, Durrington PN. The alloenzymes of
paraoxonase determine the effectiveness of high-density lipoprotein in
protecting low density lipoprotein against lipid-peroxidation. Lancet.
1997;349:851- 852.
[82] Aviram M, Hardk E, Vaya J, Mahmood S, Milo S, Hoffman A, Billicke
S, Draganov D, Rosenblat M: Human serum paraoxonase (PON1) Q and
R selectively decrease lipid peroxides in human coronary and carotid
arteriosclerotic lesions. Circulation. 2000; 101: 2510-2517.
[83] Ranade K, Kirchgessner T.G, Iakoubova O.A, Devlin J.J, Delmonte T,
Vishnupad P and at al. Evaluation of the paraoxonases as candidate
genes for stroke: Gln192Arg polymorphism 1 gene is associated with
increased risk of stroke. Strock. 2005;36:2346-2350.
[84] Ozkok E, Aydin M, Babalik E, Ozbek Z, Ince N, Kara I. Combined
impact of matrix metalloproteinase-3 andparaoxonase 1 55/192 gene
variants on coronaryartery disease in Turkish patients. Med Sci Monit.
2008; 14(10): 536-542.
[85] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in
determining normal plasma lipid and lipoprotein variation. Am J Hum
Genet 1985;37:265-8.
[86] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and
atherosclerosis. Arteriosclerosis 1988;8:1-21.
[87] Pathobiological Determinants of Atherosclerosis in Youth (PDAY)
Research Group, Hixson JE. Apolipoprotein E polymorphisms affect
atherosclerosis in young males. Arterioscler Thromb 1991;11:1237-44.
[88] Luo CC, Li WH, Moore MN, et al. Structure and evolution of the
apolipoprotein multigene family. J Mol Biol 1986;187:325-40.
[89] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and
atherosclerosis. Arteriosclerosis 1988;8:1-21.
[90] Weintraub MS, Eisenberg S, Breslow JL. Dietary fat clearance in normal
subjects is regulated by genetic variation in apolipoprotein E. J Clin
Invest 1987;80:1571-7.
[91] Hanis CL, Hewett-Emmett D, Douglas TC, et al. Effects of the
apolipoprotein E polymorphism on levels of lipids, lipoproteins, and
apolipoproteins among Mexican-Americans in Starr County, Texas.
Arterioscler Thromb 1991;11:362-70.
[92] Kataoka S, Robbins DC, Cowan LD, et al. Apolipoprotein E
polymorphism in American Indians and its relation to plasma
lipoproteins and diabetes: the Strong Heart Study. Arterioscler Thromb
Vasc Biol 1996;16:918-25.
[93] Schaefer EJ, Lamon-Fava S, Johnson S, et al. Effects of gender and
menopausal status on the association of apolipoprotein E phenotype with
plasma lipoprotein levels: results from the Framingham Offspring Study.
Arterioscler Thromb Vasc Biol 1994;14:1105-13.
[94] Hallman DM, Boerwinkle E, Saha N, et al. The apolipoprotein E
polymorphism: a comparison of allele frequencies and effects in nine
populations. Am J Hum Genet 1991;49:338-49.
[95] Lehtinen S, Lehtimaki T, Sisto T, et al. Apolipoprotein E polymorphism,
serum lipids, myocardial infarction and severity of angiography verified
coronary artery disease in men and women. Atherosclerosis
1995;114:83-91.
[96] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in
determining normal plasma lipid and lipoprotein variation. Am J Hum
Genet 1985;37:268-85.
[97] Ventakaramana P, Chengal RE and Ferrell RE. Apolipoprotein E
polymorphism in two populations of Andru Pradesh. Ind J Hum Genet
2002; 3: 1 5.
[98] Fallah S, Seifi M, Firoozrai M, Godarzi T, Jafarzadeh M, Ghohari L.H.
Influence of apo E gene polymorphism on Coronary artery disease.
Proceedings of the International Coference on Cellular and Molecular
Bioengineering; 2009 sept 23-25; Amsterdam, The Netherlands, 2009
[99] Uterman G, Hardewing A and Zimmer F. Apolipoprotein E phenotypes
in patients with myocardial infarction. Hum Genet. 1984; 65: 237-241.
[100] Lehtinens Lehtimalci T, Sisto, Salenius TP, Mikkila M and Jakela H.
Apolipoprotein E polymorphism, serum lipid, myocardial infarction and
severity of angiographically verified coronary datery disease in men and
women . Atheroscelorosis; 1995; 114: 83-91.
[101] Dembinska Kiee A, Kawecka- Jaszez K, Kwasniak M, Gaevaro I,
Pankiewicz J and Maiczewsiea Maleec M. Apo E isoforms , insulin out
put and plasma lipid levels in essential by hypertension . Eur J Clin
Invest, 1998; 28: 95-99.
[102] Yilmas H, Isbir J, Agachan B and Aydin M. Is epsilon 4 allele of
apolipoprotein E associated with more severe end stage in essential
hypertension? Cell Biochem . Funct 2001; 19: 191-195.
[103] Li X, Duy, DUY and Huang X. Association of apolipoprotein E gene
polymorphism with essential hypertension and its complication. Clin
Exp Med. 2003; 2: 175-179.
[104] Couderc R, Mahleumof, Bailleu S, Fencon G, Mary R, Fermahken J.
Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular
disease. Stroke 1993; 24: 661-664.
[105] Sealey, J.E., James, G.D., Laragh, J.H., 1995. The renin-angiotensin-
aldosterone system for normal regulation of blood pressure and sodium
and potassium homeostasis. In: Laragh, J.H., Brenner, B.M._Eds..,
Hypertension. Pathophysiology, Diagnosis and Management, vol. 2,
Raven Press, New York, NY, USA, pp. 1763-1796
[106] Hall, J.H., Mizelle, H.L., Woods, L.L., 1986. The renin-angiotensin
system and long-term regulation of blood pressure. J. Hypertens. 4, 387-
397.
[107] Dzau, V.J., 1993. Tissue renin-angiotensin system in myocardial
hypertrophy and failure. Arch. Intern. Med. 153, 937-942.
[108] Campbell, D.J., 1987. Tissue renin-angiotensin system: sites of angiotensin
formation. J. Cardiovasc. Pharmacol. 10_Suppl. 7., S1-S8.
[109] Urata, H., Nishimura, H., Ganten, D., 1996. Chymase-dependent
angiotensin II forming system in humans. Am. J. Hypertens. 9, 277-277.
[110] MacKay, J.H., Arcuri, K.E., Goldberg, A.I., Snapinn, S.M., Sweet, C.S.,
1996. Losartan and low-dose hydrochlorothiazide in patients with
essential hypertension. A double-blind placebo-controlled trial of
concomitant administration compared with individual components. Arch.
Intern. Med. 156, 278-285.
[111] Azizi, M., Guyene, T.T., Chatellier, G., Wargon, M., Me'nard, J., 1997.
Additive effects of losartan and enalapril on blood pressure and plasma
active renin. Hypertension 29, 634-640.
[112] Sharpe, N., Murphy, J., Smith, H., Hannon, S., 1988. Treatment of
patients with symptomless left ventricular dysfunction after myocardial
infarction. Lancet i, 255-259.
[113] Sharpe, N., Smith, H., Murphy, J., Greaves, S., Hart, H., Gamble, G.,
1991. Early prevention of left ventricular dysfunction after myocardial
infarction with angiotensin-converting-enzyme inhibition. Lancet 337,
872-876.
[114] Pfeffer, M.A., Braunwald, E., Moye', L.A., Basta, L., Brown, E.J. Jr.,
Cuddy, T.E., Davis, B.R., Geltman, E.M., Goldman, S., Flaker, G.C.,
Klein, M., Lamas, G.A., Packer, M., Rouleau, J., Rouleau, J.L.,
Rutherford, J., Wertheimer, J.H., Hawkins, C.M., 1992. Effect of
captopril on mortality and morbidity in patients with left ventricular
dysfunction after myocardial infarction. N. Engl. J. Med. 327, 669-677,
on behalf of the SAVE Investigators.
[115] ACE Inhibitor Myocardial Infarction Collaborative Group, 1998.
Indications for ACE inhibitors in the early treatment of acute myocardial
infarction. Systematic overview of individual data from 100,000 patients
in randomized trials. Circulation 97, 2202-2212.